Abnormal lipid metabolism is associated with angiogenic and anti angiogenic factor imbalance in PIH women

Visala Sree Jammalamadaga, Philips Abraham


Background: Preeclampsia is a major cause of maternal and fetal/neonatal mortality and morbidity even in developed countries. Despite of extensive research, the etiology and pathogenesis of preeclampsia are not completely understood. Evidence shows that imbalance between angiogenic and antiangiogenic factor plays a pivotal role in the genesis of endothelial dysfunction which is considered as a hall mark in the development of multisystem disorder in pre-eclampsia and eclampsia. Abnormal lipid metabolism is a known causative factor for endothelial dysfunction. This study has been designed to determine the association between abnormal lipids and angiogenic, anti angiogenic balance in PIH (PE and E) women.

Methods: Study group consisted of Normotensive pregnant women (N) preeclamptic women (PE) and eclamptic women (E) with 100 subjects in each group in the 3rd trimester of pregnancy. They were investigated for lipid profile and apolipoproteins, MDA, FRAP, TNF-α, sFlt-1, VEGF, PlGF, NO. Statistical analysis was done using ANOVA and pearson correlation analysis.

Results: When compared to controls TC, TGL, VLDL, LDL, apoB, MDA, TNF-α, sFlt-1 levels were found to be significantly high and HDL, apoA, FRAP, VEGF, PIGF, and NO levels were significantly low in PE, E group.  Eclamptic women showed a significantly high level of MDA, TNF-α, sFlt-1and low levels of FRAP, VEGF, PIGF, NO when compared to PE group.

Conclusions: In PIH women, abnormal lipid metabolism is associated with angiogenic and antiangiogenic imbalance.


Angiogenic and anti-angiogenic factors, Eclamptic women, Lipids, Preeclamptic women

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Kintiraki E, Papakatsika S, Kotronis G, Goulis DG, Kotsis V. Pregnancy-induced hypertension: review. Hormones. 2015;14(2):211-23.

Hubel CA. Oxidative stress in the pathogenesis of preeclampsia. Proc Soc Exp Biol Med. 1999;222(3):222-35

Hansson SR, Nääv Å, Erlandsson L. Oxidative stress in preeclampsia and the role of free fetal hemoglobin. Frontiers in physiology. 2014;5.

Program NH. Report of the national high blood pressure education program working group on high blood pressure in pregnancy, national high blood pressure education program working group on high blood pressure in pregnancy. Am J Obstet Gynecol. 2000;183(1):S1-S22.

Sajith M, Nimbargi V, Modi A, Sumariya R, Pawar A. Incidence of pregnancy induced hypertension and prescription pattern of antihypertensive drugs in pregnancy. Int J Pharma Sci Res. 2014;23:4.

Granger JP. Role of endothelial dysfunction in pregnancy-induced hypertension. Am J Hypertens. 2000;13(S2):324A

Lorentzen B. Plasma lipids and vascular dysfunction in preeclampsia. Semin Reprod Endocrinol. 1998;16(1):339.

Catalano PM. Obesity, insulin resistance, and pregnancy outcome. Reproduction. 2010;140(3):365-71.

Soca PEM. Dyslipidemia in preeclampsia syndrome. Cor Salud. 2013;5(2):221-5.

Phalak P, Tilak M. Study of lipid profile in pre-eclampsia. Indian J Basic Appl Med Res. 2012;5(2):405-9.

Maartje E. Apolipoprotein B synthesis inhibition: results from clinical trials. Curr Opinion Lipidol. 2010;21:319-323.

Ekhator CN, Ebomoyi MI. Blood glucose and serum lipid profiles during pregnancy. Afr J Diab Med. 2012;20(1).

Kaloti AS, Kaur C, Goel RK, Jha S. Lipid profile trends in women of pregnancy induced hypertension cases in a rural setup. JEMDS. 2013;2(13):2024:31.

Owiredu WK. Lipid profile and lipid peroxidation among Ghanaian pregnancy-induced hypertensives. J Med Sci. 2008;8(8):691-8.

Adeniji AO, Oparinde DP. Comparison of lipid peroxidation and anti-oxidant ac-tivities in pre-eclamptic and normal pregnancies in Nigerian Population. Int J Clin Med. 2013;4(05):239.

Hung TH, Charnock-Jones DS, Skepper JN, Burton GJ. Secretion of tumor necrosis factor-α from human placental tissues induced by hypoxia-reoxygenation causes endothelial cell activation in vitro: a potential mediator of the inflammatory response in preeclampsia. Am J Pathol. 2004;164(3):1049-61.

Murphy SR, LaMarca BB, Parrish M, Cockrell K, Granger JP. Control of soluble fms-like tyrosine-1 (sFlt-1) production response to placental ischemia/hypoxia: role of tumor necrosis factor-α. Am J Physiol Regul Integr Comp Physiol. 2013;304:R130-5.

Luttun A, Carmeliet P. Soluble VEGF receptor Flt1: the elusive preeclampsia factor discovered? J Clin Invest. 2003;111(5):600.

Stepan H, Geide A, Faber R. Soluble fms like tyrosine kinase-1. N Engl J Med. 2004;351:2241-2.

Lee ES, Oh MJ, Jung JW, Lim JE, Seol HJ, Lee KJ, Kim HJ. The levels of circulating vascular endothelial growth factor and soluble Flt-1 in pregnancies complicated by preeclampsia. J Korean Med Sci. 2007;22(1):94-8.

Müller-Deile J, Schiffer M. Renal involvement in preeclampsia: similarities to VEGF ablation therapy. Journal of pregnancy. 2010;2011.

Khvorova A, Moore M, Turanov AA, Karumanchi A. United States Patent, Karumanchi, Beth Israel Deconess Medical Center, May 13, 2013.

Shen BQ, Lee DY, Zioncheck TF. Vascular endothelial growth factor governs endothelial nitric-oxide synthase expression via a KDR/Flk-1 receptor and a protein kinase C signaling pathway. J Biologic Chem. 1999;274(46):33057-63.

Sankaralingam S, Xu Y, Sawamura T, Davidge ST. Increased lectin-like oxidized low-density lipoprotein receptor-1 expression in the maternal vasculature of women with preeclampsia. Hypertension. 2009;53(2):270-7.